Fusafungine, also known as fusafungin, is a cyclic depsipeptide antibiotic from Fusarium lateririum used for the treatment of nasal and throat infection including sinusitis, rhinitis, rhinopharyngitis, angina, laryngitis, and tracheitis. Fusafungine consists of a mixture of enniatins and has been widely used over the past 50 years. Its first authorization in the EU was in 1963. Fusafungine showed bacteriostatic activity against a suite of microorganisms, such as Mycoplasma pneumoniae, Legionella pneumophila, Streptococcus pneumoniae, S. pyogenes, and Staphylococcus aureus, including methicillin-resistant S. aureus. Besides its bacteriostatic activity against most micro-organisms involved in respiratory tract infections fusafungine displays original anti-inflammatory properties. Fusafungine has multiple mechanisms of action, including downregulation of the expression of intercellular adhesion molecule-1 (ICAM-1) and inhibition of production of proinflammatory cytokines. In September 2015, an EU-wide assessment of the benefit-risk of fusafungine was initiated due to an increase in the reporting rate of serious allergic reactions. European Medicines Agency (EMA) Pharmacovigilance Risk Assessment Committee (PRAC) recommended that fusafungine should be withdrawn from the EU market

Fencamfamin is a camphane derivative, although lacking typical sympathomimetic properties. It is structurally related to the phenylethylamines. It is a central nervous stimulant with pharmacological properties similar to amphetamine. Fencamfamin developed primarily as appetite suppressant or pscyhostimulant, not to increase awareness. Fencamfamin reduces REM sleep and prevents fatigue in subjects deprived of sleep. Fencamfamin raises a mood.

Spiramycin, a macrolide antibiotic, has been studied in the United States for the treatment of cryptosporidial diarrhea. Some reports suggest that spiramycin is useful in improving the symptoms of cryptosporidial diarrhea in some patients. It has been used in Europe and Canada for over 20 years to treat bacterial infections. Serious adverse effects from spiramycin are apparently rare, and no drug-associated deaths have been reported. Spiramycin inhibits translocation by binding to bacterial 50S ribosomal subunits with an apparent 1:1 stoichiometry. This antibiotic is a potent inhibitor of the binding to the ribosome of both donor and acceptor substrates. Spiramycin induces rapid breakdown of polyribosomes, an effect which has formerly been interpreted as occurring by normal ribosomal run-off followed by an antibiotic-induced block at or shortly after initiation of a new peptide. However, there is now convincing evidence that spiramycin, and probably all macrolides, act primarily by stimulating the dissociation of peptidyl-tRNA from ribosomes during translocation